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Nectin-like Molecule 1 Inhibits the Migration and Invasion of U251 Glioma Cells by Regulating the Expression of An extracellular matrix protein Osteopontin

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Chinese Medical Sciences Journal 2010年第2期25卷 100-104页

作者： Bin Yin Ke-han Li Tai An Tao Chen Xiao-zhong Peng National Laboratory of Medical Molecular Biology Institute of Basic Medical Sciences Chinese Academy of Medical Sciences ＆ Peking Union Medical College Beijing 100005 China

Objective To investigate the molecular mechanism of nectin-like molecule 1(NECL1) inhibiting the migration and invasion of U251 glioma *** We infected U251 glioma cells with adeno-nectin-like molecule 1(Ad-NECL1) or empty adenovirus(Ad).Transwell and wound healing assays were performed to observe the migration of U251 cells incubated with the cell supernatant from Ad-NECL1 or Ad infected U251 *** microarray was applied to screen the gene expression profile after the restoration of NECL1 in U251 glioma cell *** differential expression of osteopontin(OPN),a gene related to migration and invasion,was further analyzed with semi-quantitative reverse transcription-polymerase chain reaction(RT-PCR),Western blot,and *** The restoration of NECL1 inhibited migration of U251 cells significantly(Pextracellular matrix proteins involved in the migration of *** mRNA and protein expressions of OPN,the most markedly reduced extracellular matrix protein,were found decreased in U251 cells after restoration of *** assay also detected an increase of OPN in glioma tissues,related with the progressing of malignant *** A link might exist between NECL1 and the extracellular matrix protein OPN in inhibiting the migration and invasion of U251 glioma cells.

关键词： nectin-like molecule 1 glioma cell line extracellular matrix protein osteopontin

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Comparative proteomic analysis of extracellular matrix proteins secreted by hypertrophic scar witb normal skin fibroblasts

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Burns & Trauma 2014年第2期2卷 76-83页

作者： Li Ma Chengjun Gan Yong Huang Ying Wang Gaoxing Luo Jun Wu Chongqing Key Laboratory for Disease Proteomics State Key Laboratory of Trauma Burns and Combined Injury Institute of Burn Research Southwest Hospital the Third Military Medical University Chongqing School of Environmental Air Security and Pollution Control Engineering Jinan University Guangzhou Chongqing Key Laboratory for Disease Proteomics State Key Laboratory of Trauma Burns and Combined Injury Institute of Burn Research Southwest Hospital the Third Military Medical University Chongqing The 421 Hospital People's Liberation Army Guangzhou China Chongqing Key Laboratory for Disease Proteomics State Key Laboratory of Trauma Burns and Combined Injury Institute of Burn Research Southwest Hospital the Third Military Medical University Chongqing

The formation of hypertrophic scars (HSs) is a fibroproliferative disorder of abnormal wound healing. HSs usually characterize excessive proliferation of fibroblasts, abnormal deposition of extracellular matrix (ECM) during wound healing, associated with cosmetic, functional, and psychological problems. Owing to the role of ECM proteins in scar formation, we comparatively analyzed matrix proteins secreted by normal skin fibroblasts (NSFs) and HS fibroblasts (HSFs). The acetone-extracted secreted proteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), and identified by mass spectrometry (MS). Based on Go annotation of MS data, the profiling of ECM proteins was established and scar-related proteins have been screened out. The functions of several ECM proteins identified by MS have been discussed, such as collagens I, VI, XII, fibronectin, decorin, lumican, and protein procollagen C endopeptidase enhancer 1 (PCPE-1). Among them, the MS result of PCPE-1 was supported by Western blotting that PCPE-1 from HSFs were significantly upregulated than that from NSFs. It is suggested that PCPE-1 could be a potential target for scar treatment. The exploration of scar related proteins may provide new perspectives on understanding the mechanism of scar formation and open a new way to scar treatment and prevention.

关键词： extracellular matrix protein fibroblast proteomics hypertrophic scar

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Role of activin receptor-like kinase 1 in vascular development and cerebrovascular diseases

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Neural Regeneration Research 2020年第10期15卷 1807-1813页

作者： Jun-Mou Hong Yi-Da Hu Xiao-Qing Chai Chao-Liang Tang Department of Vascular Surgery Zhongshan HospitalXiamen UniversityXiamenFujian ProvinceChina Department of Anesthesiology Renmin Hospital of Wuhan UniversityWuhanHubei ProvinceChina Department of Anesthesiology The First Affiliated Hospital of USTCDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefeiAnhui ProvinceChina

Activin receptor-like kinase 1(ALK1)is a transmembrane serine/threonine receptor kinase of the transforming growth factor beta(TGFβ)receptor ***1 is specifically expressed in vascular endothelial cells,and its dynamic changes are closely related to the proliferation of endothelial cells,the recruitment of pericytes to blood vessels,and functional differentiation during embryonic vascular *** pathophysiology of many cerebrovascular diseases is today understood as a disorder of endothelial cell function and an imbalance in the proportion of vascular ***,mutations in ALK1 and its co-receptor endoglin are major genetic risk factors for vascular arteriovenous *** studies have shown that ALK1 is closely related to the development of cerebral aneurysms,arteriovenous malformations,and cerebral *** this review,we describe the various roles of ALK1 in the regulation of angiogenesis and in the maintenance of cerebral vascular homeostasis,and we discuss its relationship to functional dysregulation in cerebrovascular *** review should provide new perspectives for basic research on cerebrovascular diseases and offer more effective targets and strategies for clinical diagnosis,treatment,and prevention.

关键词： activin receptor-like kinase 1 aneurysm atherosclerotic plaque endoglin extracellular matrix protein intracranial arteriovenous malformation matrix metalloproteinase pericyte transforming growth factor beta 1 pathway vascular development

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Role of angiogenesis and angiogenic factors in acute and chronic wound healing

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Plastic and Aesthetic Research 2015年第1期2卷 243-249页

作者： Thittamaranahalli Muguregowda Honnegowda Pramod Kumar Echalasara Govindarama Padmanabha Udupa Sudesh Kumar Udaya Kumar Pragna Rao Department of Plastic Surgery and Burns Kasturba Medical CollegeManipal 576104KarnatakaIndia Department of Plastic Surgery King Abdulaziz Specialist HospitalSakaka 42421Al-JoufSaudi Arabia Department of Biochemistry Kasturba Medical CollegeManipal 576104KarnatakaIndia Department of Surgery District Government HospitalUdupi 576108KarnatakaIndia

Angiogenesis plays a crucial role in wound healing by forming new blood vessels from preexisting vessels by invading the wound clot and organizing into a microvascular network throughout the granulation *** dynamic process is highly regulated by signals from both serum and the surrounding extracellular matrix *** endothelial growth factor,angiopoietin,fibroblast growth factor and transforming growth factor-beta are among the potent angiogenic cytokines in wound *** endothelial cell ECM receptors are critical for morphogenetic changes in blood vessels during wound *** particular integrin(αvβ3)receptors for fibrin and fibronectin,appear to be required for wound angiogenesis:αvβ3 is focally expressed at the tips of angiogenic capillary sprouts invading the wound clot,and any functional inhibitors ofαvβ3 such as monoclonal antibodies,cyclic RGD peptide antagonists,and peptidomimetics rapidly inhibit granulation tissue *** spite of clear knowledge about influence of many angiogenic factors on wound healing,little progress has been made in defining the source of these factors,the regulatory events involved in wound angiogenesis and in the clinical use of angiogenic stimulants to promote repair.

关键词： Angiogenic factors endothelium extracellular matrix protein granulation tissue wound healing

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FN对LAK细胞活性的增强作用及机理(英文)

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中国肿瘤生物治疗杂志 1997年第1期4卷 26-34页

作者： LiY KobayashiM KuramitsuY CancerInstitute HokkaidoUniversitySchoolofMedicine Japan Kita-15 Kita-ku Laboratoryofpathology Nishi-7 Sapporo060

本研究探讨了FN对LAK细胞活性的影响.extracellular matrix protein(ECM)中的一种成分FN是基底膜、细胞间质及细胞表面的重要组成成分.本文发现FN能调节LAK细胞的功能.首先、LAK细胞和FN的粘付能力被增强.第二、经过与FN共同培养的LAK... 详细信息

本研究探讨了FN对LAK细胞活性的影响.extracellular matrix protein(ECM)中的一种成分FN是基底膜、细胞间质及细胞表面的重要组成成分.本文发现FN能调节LAK细胞的功能.首先、LAK细胞和FN的粘付能力被增强.第二、经过与FN共同培养的LAK细胞活性比正常要高15～20%左右.FN对LAK细胞活性增强机理是通过激活LAK细胞表面的LFA-1的活性(不是LFA-1数量的增加)来增强LAK细胞和肿瘤细胞的结合功能、提高LAK细胞的杀伤肿瘤细胞的能力.本文的结果表明FN-LAK可能会改善肿瘤治疗效果、并间接提示肿瘤细胞表面及肿瘤组织中的FN成分的多少可直接影响LAK细胞的治疗效果.

关键词： lymphokine activated killer(LAK) activity extracellular matrix protein adhesion molecule

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